Essentials of strength training and conditioning / National Strength and Conditioning Association ; G. Gregory Haff, N. Travis Triplett, editors. -- Fourth edition. p. ; cm. Includes bibliographical references and index. I. Haff, Greg, editor. II. Triplett, N. Travis, 1964- , editor. III. National Strength & Conditioning Association (U.S.), issuing body. [DNLM: 1. Physical Education and Training--methods. 2. Athletic Performance--physiology. 3. Physical Conditioning, Human--physiology. 4. Physical Fitness--physiology. 5. Resistance Training--methods. QT 255] GV711.5 613.7'1--dc23 2014047045 ISBN: 978-1-4925-0162-6 Copyright © 2016, 2008, 2000, 1994 by the National Strength and Conditioning Association All rights reserved. Except for use in a review, the reproduction or utilization of this work in any form or by any electronic, mechanical, or other means, now known or hereafter invented, including xerography, photocopying, and recording, and in any information storage and retrieval system, is forbidden without the written permission of the publisher. Notice: Permission to reproduce the following material is granted to individuals and agencies who have purchased Essentials of Strength Training and Conditioning, Fourth Edition: pp. 636, 637-639, 645. The reproduction of other parts of this book is expressly forbidden by the above copyright notice. Persons or agencies who have not purchased Essentials of Strength Training and Conditioning, Fourth Edition, may not reproduce any material. Permission notices for material reprinted in this book from other sources can be found on pages xv-xvi. The web addresses cited in this text were current as of April 2015, unless otherwise noted.
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CONTENTS Preface vii Accessing the Lab Activities xi Acknowledgments xiii Credits xv CHAPTER 1 Structure and Function of Body Systems 1 N. Travis Triplett, PhD Musculoskeletal System 2 • Neuromuscular System 8 • Cardiovascular System 12 • Respiratory System 15 • Conclusion 17 • Learning Aids 17 CHAPTER 2 Biomechanics of Resistance Exercise 19 Jeffrey M. McBride, PhD Skeletal Musculature 20 • Anatomical Planes and Major Body Movements 25 • Human Strength and Power 25 • Sources of Resistance to Muscle Contraction 33 • Joint Biomechanics: Concerns in Resistance Training 37 • Conclusion 40 • Learning Aids 41 CHAPTER 3 Bioenergetics of Exercise and Training 43 Trent J. Herda, PhD, and Joel T. Cramer, PhD Essential Terminology 44 • Biological Energy Systems 44 • Substrate Depletion and Repletion 55 • Bioenergetic Limiting Factors in Exercise Performance 56 • Oxygen Uptake and the Aerobic and Anaerobic Contributions to Exercise 57 • Metabolic Specificity of Training 59 • Conclusion 61 • Learning Aids 62 CHAPTER 4 Endocrine Responses to Resistance Exercise 65 William J. Kraemer, PhD, Jakob L. Vingren, PhD, and Barry A. Spiering, PhD Synthesis, Storage, and Secretion of Hormones 66 • Muscle as the Target for Hormone Interactions 69 • Role of Receptors in Mediating Hormonal Changes 69 • Categories of Hormones 70 • Heavy Resistance Exercise and Hormonal Increases 72 • Mechanisms of Hormonal Interactions 72 • Hormonal Changes in Peripheral Blood 73 • Adaptations in the Endocrine System 73 • Primary Anabolic Hormones 74 • Adrenal Hormones 82 • Other Hormonal Considerations 84 • Conclusion 85 • Learning Aids 86 www.ebook3000.com
iv ChaptEr 5 Adaptations to Anaerobic Training Programs 87 Duncan French, PhD Neural Adaptations 88 • Muscular Adaptations 93 • Connective Tissue Adaptations 97 • Endocrine Responses and Adaptations to Anaerobic Training 102 • Cardiovascular and Respiratory Responses to Anaerobic Exercise 103 • Compatibility of Aerobic and Anaerobic Modes of Training 105 • Overtraining 107 • Detraining 110 • Conclusion 111 • Learning Aids 112 ChaptEr 6 Adaptations to Aerobic Endurance Training Programs 115 Ann Swank, PhD, and Carwyn Sharp, PhD Acute Responses to Aerobic Exercise 116 • Chronic Adaptations to Aerobic Exercise 120 • Adaptations to Aerobic Endurance Training 124 • External and Individual Factors Influencing Adaptations to Aerobic Endurance Training 124 • Overtraining: Definition, Prevalence, Diagnosis, and Potential Markers 129 • Conclusion 132 • Learning Aids 133 ChaptEr 7 Age- and Sex-Related Differences and Their Implications for Resistance Exercise 135 Rhodri S. Lloyd, PhD, and Avery D. Faigenbaum, EdD Children 136 • Female Athletes 144 • Older Adults 148 • Conclusion 153 • Learning Aids 154 ChaptEr 8 Psychology of Athletic Preparation and Performance 155 Traci A. Statler, PhD, and Andrea M. DuBois, MS Role of Sport Psychology 156 • Ideal Performance State 156 • Energy Management: Arousal, Anxiety, and Stress 157 • Influence of Arousal and Anxiety on Performance 158 • Motivation 161 • Attention and Focus 163 • Psychological Techniques for Improved Performance 164 • Enhancing Motor Skill Acquisition and Learning 169 • Conclusion 172 • Learning Aids 173 ChaptEr 9 Basic Nutrition Factors in Health 175 Marie Spano, MS, RD Role of Sports Nutrition Professionals 176 • Standard Nutrition Guidelines 178 • Macronutrients 181 • Vitamins 190 • Minerals 193 • Fluid and Electrolytes 196 • Conclusion 199 • Learning Aids 200 ChaptEr 10 Nutrition Strategies for Maximizing Performance 201 Marie Spano, MS, RD Precompetition, During-Event, and Postcompetition Nutrition 202 • Nutrition Strategies for Altering Body Composition 216 • Feeding and Eating Disorders 221 • Conclusion 224 • Learning Aids 224 ChaptEr 11 Performance-Enhancing Substances and Methods 225 Bill Campbell, PhD Types of Performance-Enhancing Substances 226 • Hormones 228 • Dietary Supplements 237 • Conclusion 247 • Learning Aids 248 www.ebook3000.com
ChaptEr 12 Principles of Test Selection and Administration 249 Michael McGuigan, PhD Reasons for Testing 250 • Testing Terminology 250 • Evaluation of Test Quality 250 • Test Selection 253 • Test Administration 254 • Conclusion 257 • Learning Aids 258 ChaptEr 13 Administration, Scoring, and Interpretation of Selected Tests 259 Michael McGuigan, PhD Measuring Parameters of Athletic Performance 260 • Selected Test Protocols and Scoring Data 264 • Statistical Evaluation of Test Data 291 • Conclusion 293 • Learning Aids 294 ChaptEr 14 Warm-Up and Flexibility Training 317 Ian Jeffreys, PhD Warm-Up 318 • Flexibility 320 • Types of Stretching 323 • Conclusion 328 • Static Stretching Techniques 329 • Dynamic Stretching Techniques 341 • Learning Aids 350 ChaptEr 15 Exercise Technique for Free Weight and Machine Training 351 Scott Caulfield, BS, and Douglas Berninger, MEd Fundamentals of Exercise Technique 352 • Spotting Free Weight Exercises 354 • Conclusion 357 • Resistance Training Exercises 358 • Learning Aids 408 ChaptEr 16 Exercise Technique for Alternative Modes and Nontraditional Implement Training 409 G. Gregory Haff, PhD, Douglas Berninger, MEd, and Scott Caulfield, BS General Guidelines 410 • Bodyweight Training Methods 410 • Core Stability and Balance Training Methods 411 • Variable-Resistance Training Methods 413 • Nontraditional Implement Training Methods 417 • Unilateral Training 421 • Conclusion 421 • Modes and Nontraditional Exercises 422 • Learning Aids 438 ChaptEr 17 Program Design for Resistance Training 439 Jeremy M. Sheppard, PhD, and N. Travis Triplett, PhD Principles of Anaerobic Exercise Prescription 440 • Step 1: Needs Analysis 441 • Step 2: Exercise Selection 443 • Step 3: Training Frequency 447 • Step 4: Exercise Order 448 • Step 5: Training Load and Repetitions 451 • Step 6: Volume 462 • Step 7: Rest Periods 465 • Conclusion 467 • Learning Aids 469 ChaptEr 18 Program Design and Technique for Plyometric Training 471 David H. Potach, PT, and Donald A. Chu, PhD, PT Plyometric Mechanics and Physiology 472 • Program Design 475 • Age Considerations 478 • Plyometrics and Other Forms of Exercise 480 • Safety Considerations 481 • Conclusion 482 • Plyometric Drills 483 • Learning Aids 520 www.ebook3000.com
vi ChaptEr 19 Program Design and Technique for Speed and Agility Training 521 Brad H. DeWeese, EdD, and Sophia Nimphius, PhD Speed and Agility Mechanics 522 • Neurophysiological Basis for Speed 525 • Running Speed 527 • Agility Performance and Change-of-Direction Ability 533 • Methods of Developing Speed 536 • Methods of Developing Agility 538 • Program Design 539 • Speed Development Strategies 541 • Agility Development Strategies 545 • Conclusion 547 • Speed and Agility Drills 548 • Learning Aids 557 ChaptEr 20 Program Design and Technique for Aerobic Endurance Training 559 Benjamin H. Reuter, PhD, and J. Jay Dawes, PhD Factors Related to Aerobic Endurance Performance 560 • Designing an Aerobic Endurance Program 561 • Types of Aerobic Endurance Training Programs 567 • Application of Program Design to Training Seasons 570 • Special Issues Related to Aerobic Endurance Training 571 • Conclusion 573 • Aerobic Endurance Training Exercises 574 • Learning Aids 581 ChaptEr 21 Periodization 583 G. Gregory Haff, PhD Central Concepts Related to Periodization 584 • Periodization Hierarchy 587 • Periodization Periods 588 • Applying Sport Seasons to the Periodization Periods 592 • Undulating Versus Linear Periodization Models 593 • Example of an Annual Training Plan 593 • Conclusion 595 • Learning Aids 604 ChaptEr 22 Rehabilitation and Reconditioning 605 David H. Potach, PT, and Terry L. Grindstaff, PhD, PT, ATC Sports Medicine Team 606 • Types of Injury 608 • Tissue Healing 610 • Goals of Rehabilitation and Reconditioning 611 • Program Design 616 • Reducing Risk of Injury and Reinjury 618 • Conclusion 620 • Learning Aids 621 ChaptEr 23 Facility Design, Layout, and Organization 623 Andrea Hudy, MA General Aspects of New Facility Design 624 • Existing Strength and Conditioning Facilities 625 • Assessing Athletic Program Needs 625 • Designing the Strength and Conditioning Facility 627 • Arranging Equipment in the Strength and Conditioning Facility 628 • Maintaining and Cleaning Surfaces and Equipment 630 • Conclusion 631 • Learning Aids 633 ChaptEr 24 Facility Policies, Procedures, and Legal Issues 641 Traci Statler, PhD, and Victor Brown, MS Mission Statement and Program Goals 642 • Program Objectives 642 • Strength and Conditioning Performance Team 643 • Legal and Ethical Issues 647 • Staff Policies and Activities 651 • Facility Administration 653 • Emergency Planning and Response 653 • Conclusion 655 • Learning Aids 656 Answers to Study Questions 657 References 659 Index 721 About the Editors 731 Contributors 733 Contributors to Previous Editions 735 www.ebook3000.com
PREFACE In 1994, the first edition of Essentials of Strength Train- ing and Conditioning was published. After a second edition (in 2000) and sales of over 100,000 books, an expanded and updated third edition was published in 2008. This newest edition continues the tradition as the most comprehensive reference available for strength and conditioning professionals. In this text, 30 expert contributors further explore the scientific principles, concepts, and theories of strength training and condi- tioning and their applications to athletic performance.
The first edition grew out of an awareness that there was not a book about strength training and condition- ing that captured the views of leading professionals in anatomy, biochemistry, biomechanics, endocrinology, nutrition, exercise physiology, psychology, and the other sciences and that related the principles from these disciplines to the design of safe and effective training programs. Also, the lack of relevant and well-conducted research studies had hindered earlier efforts to create an all-inclusive resource. Once it was finally developed, Essentials of Strength Training and Conditioning quickly became the definitive textbook on the subject.
The second edition, released six years later, was more than a simple freshening of the content; it was an overhaul of the scope and application of the first edi- tion. Throughout the text and in the additional 100-plus pages, the chapter contributors used updated, relevant, and conclusive research and concepts to turn scientific information into information on performance. Many learning tools were added, such as chapter objectives, key points, application boxes, and sample resistance training programs for three different sports. These enhancements, plus the addition of a full-color interior and hundreds of color photographs, made the second edition truly exceptional.
The third edition, released eight years after the second edition, offered restructured chapters and expansions of other chapters complete with new photographs and updated terminology. In addition, the artwork was mod- ernized and instructor and student resources were created to help keep this text the primary resource for the study and instruction of strength and conditioning. Updates to the Fourth Edition This fourth edition expands on the earlier editions and applies the most current research and information in a logical format that reaffirms Essentials of Strength Training and Conditioning as the most prominent resource for students preparing for careers in strength and conditioning and for sport science professionals involved in training athletes. The primary enhancements are as follows: • Online videos featuring 21 resistance training exercises demonstrate proper exercise form for classroom and practical use. • Updated research—specifically in the areas of high-intensity interval training, overtraining, agility and change of direction, nutrition for health and performance, and periodization—helps readers better understand these popular trends in the industry. • A new chapter with instructions and photos pres- ents techniques for exercises using alternative modes and nontraditional implements. • Ten additional tests, including tests for maximum strength, power, and aerobic capacity, along with new flexibility exercises, resistance training exer- cises, plyometric exercises, and speed and agility drills, help professionals design programs that reflect current guidelines.
These enhancements, plus an expanded ancillary package for instructors including a new, robust collec- tion of more than 60 instructor videos demonstrating resistance training, plyometric exercises, and alter- native mode exercises, brings practical content to the classroom. Working along with the instructor guide and presentation package, a test package has been added to assist instructors in evaluating students’ understanding of key concepts.
Each chapter begins with objectives and includes key points to guide the reader along the way. Key terms are boldfaced and listed at the end of the chapter. Chapters www.ebook3000.com
viii include sidebars that apply the content, and later chap- ters include sample resistance training programs for three different sports. Detailed instructions and photos are provided for testing, stretching, resistance training, alternative modes, plyometrics, agility training, and aerobic endurance exercise. Finally, chapters end with multiple-choice study questions, with an answer key at the end of the book. Instructor Resources In addition to the updated content, this edition includes newly created instructor resources: •Instructor Video. The instructor video includes video of correct technique for 61 resistance training, alternative, and plyometric exercises. These can be used for demonstration, lecture, and discussion. •Instructor Guide. The instructor guide contains a course description, a sample semester schedule, chapter objectives, chapter outlines, key terms with definitions, and application questions with answers. •Presentation Package and Image Bank. This comprehensive resource, delivered in Microsoft PowerPoint, offers instructors a presentation package containing over 1,300 slides to help aug- ment lectures and class discussions. In addition to outlines and key points, the resource contains more than 600 figures, tables, and photos from the textbook, which can be used as an image bank by instructors who need to customize their presen- tations. Easy-to-follow instructions help guide instructors on how to reuse the images within their own PowerPoint templates. •Test Package. The test package includes a bank of 240 multiple-choice questions, from which instructors can make their own tests and quizzes. Instructors can download Respondus or RTF files or files formatted for use in a learning manage- ment system.
These instructor resources can be found at www.Human Kinetics.com/EssentialsOfStrengthTrainingAnd Conditioning. Essentials of Strength Training and Conditioning 8 double helix. The myosin crossbridge now attaches much more rapidly to the actin filament, allowing force to be produced as the actin filaments are pulled toward the center of the sarcomere (1). It is important to understand that the amount of force produced by a muscle at any instant in time is directly related to the number of myosin crossbridges bound to actin filaments cross-sectionally at that instant in time (1). ▶The number of crossbridges that are formed
between actin and myosin at any instant
in time dictates the force production of a
muscle.Contraction Phase The energy for pulling action, or power stroke, comes from hydrolysis (breakdown) of adenosine triphosphate (ATP) to adenosine diphos- phate (ADP) and phosphate, a reaction catalyzed by the enzyme myosin adenosine triphosphatase (ATPase). Another molecule of ATP must replace the ADP on the myosin crossbridge globular head in order for the head to detach from the active actin site and return to its original position. This allows the contraction process to continue (if calcium is available to bind to troponin) or relaxation to occur (if calcium is not available). It may be noted that calcium plays a role in regulating a large number of events in skeletal muscle besides contraction. These include glycolytic and oxidative energy metabolism, as well as protein synthesis and degradation (10). ▶Calcium and ATP are necessary for cross-
bridge cycling with actin and myosin fila-
ments.Recharge Phase Measurable muscle shortening transpires only when this sequence of events—binding of calcium to troponin, coupling of the myosin cross- bridge with actin, power stroke, dissociation of actin and myosin, and resetting of the myosin head position—is repeated over and over again throughout the muscle fiber. This occurs as long as calcium is available in the myofibril, ATP is available to assist in uncoupling the myosin from the actin, and sufficient active myosin ATPase is available for catalyzing the breakdown of ATP. Relaxation Phase Relaxation occurs when the stim- ulation of the motor nerve stops. Calcium is pumped back into the sarcoplasmic reticulum, which prevents the link between the actin and myosin filaments. Relaxation is brought about by the return of the actin and myosin filaments to their unbound state. Neuromuscular System Muscle fibers are innervated by motor neurons that trans- mit impulses in the form of electrochemical signals from the spinal cord to muscle. A motor neuron generally has numerous terminal branches at the end of its axon and thus innervates many different muscle fibers. The whole structure is what determines the muscle fiber type and its characteristics, function, and involvement in exercise. Activation of Muscles When a motor neuron fires an impulse or action poten- tial, all of the fibers that it serves are simultaneously activated and develop force. The extent of control of a muscle depends on the number of muscle fibers within each motor unit. Muscles that must function with great precision, such as eye muscles, may have motor units with as few as one muscle fiber per motor neuron. Changes in the number of active motor units in these small muscles can produce the extremely fine gradations in force that are necessary for precise movements of the eyeball. In contrast, the quadriceps muscle group, which moves the leg with much less precision, may have sev- eral hundred fibers served by one motor neuron. Steps of Muscle Contraction
The steps of muscle contraction can be summarized as follows:1. Initiation of ATP splitting (by myosin ATPase) causes myosin head to be in an “energized” state that allows it to move into a position to be able to form a bond with actin. 2. The release of phosphate from the ATP splitting process then causes the myosin head to change shape and shift. 3. This pulls the actin lament in toward the center of the sarcomere and is referred to as the power stroke; ADP is then released. 4. Once the power stroke has occurred, the myosin head detaches from the actin but only after another ATP binds to the myosin head because the binding process facilitates detachment. 5. The myosin head is now ready to bind to another actin (as described in step 1), and the cycle contin- ues as long as ATP and ATPase are present and calcium is bound to the troponin. 374 15.15 FLAT DUMBBELL FLY (and Incline Variation) Chest This exercise can also be performed on an incline bench. If using the incline variation, begin by position- ing the dumbbells over the head and face instead of over the chest. Starting Position: Athlete • Grasp two dumbbells using a closed, neutral grip. • Lie in a supine position on a bench in the five- point body contact position. • Signal the spotter for assistance in moving the dumbbells into the starting position. • Press the dumbbells in unison to an extended-el- bow position above the chest. • Slightly flex the elbows and point them out to the sides. • All repetitions begin from this position. Starting Position: Spotter • Position one knee on the floor with the foot of the other leg forward and flat on the floor (or kneel on both knees). • Grasp the athlete’s forearms near the wrists. • At the athlete’s signal, assist with moving the dumbbells to a position over the athlete’s chest. • Release the athlete’s forearms smoothly. Downward Movement Phase: Athlete • Lower the dumbbells in a wide arc until they are level with the shoulders or chest. • Keep the dumbbell handles parallel to each other as the elbows move downward. • Keep the wrists stiff and the elbows held in a slightly flexed position. • Keep the hands, wrists, forearms, elbows, upper arms, and shoulders in the same vertical plane. • Maintain the five-point body contact position. Downward Movement Phase: Spotter • Keep the hands near—but not touching—the athlete’s forearms near the wrists as the dumb- bells descend. Upward Movement Phase: Athlete • Raise the dumbbells up toward each other in a wide arc back to the starting position. • Keep the wrists stiff and the elbows held in a slightly flexed position. • Keep the hands, wrists, forearms, elbows, upper arms, and shoulders in the same vertical plane. • Maintain the five-point body contact position. Upward Movement Phase: Spotter • Keep the hands near—but not touching—the athlete’s forearms near the wrists as the dumb- bells ascend. Starting positions Downward and upward movements MAJOR MUSCLES INVOLVED pectoralis major, anterior deltoids Sidebars Key points Exercise photos Video available online www.ebook3000.com
Student and Professional Resources The web resource with online video includes video of 21 resistance training exercises for use in understanding and performing correct exercise technique. Lab activities are provided to give students hands-on practice with testing and evaluation. The fillable forms make completing and submitting lab assignments easy.
The web resource can be found at www.HumanKinetics .com/EssentialsOfStrengthTrainingAndConditioning. Certification Exams Essentials of Strength Training and Conditioning is the primary resource for individuals preparing for the National Strength and Conditioning Association’s Certified Strength and Conditioning Specialist (CSCS) certification exam.
As a worldwide authority on strength and condition-ing, the National Strength and Conditioning Association Essentials of Strength Training and Conditioning 86 body and helping with the adaptive response to heavy resistance training. Whether trying to optimize a work- out or avoid overtraining, the strength and conditioning professional must remember that the endocrine system plays an important role. The goal of this chapter has been to provide an initial glimpse into this complex but also highly organized system that helps to mediate changes in the body with resistance exercise training. KEY TERMS allosteric binding site anabolic hormone catabolic hormone cross-reactivity diurnal variation downregulation endocrine gland General Adaptation Syndrome hormone hormone–receptor complex (H-RC) lock-and-key theory neuroendocrine immunology neuroendocrinology polypeptide hormone proteolytic enzyme secondary messenger steroid hormone target tissue cell thyroid hormone STUDY QUESTIONS 1. After a bout of resistance training, acute hormonal secretions provide all of the following information to the body EXCEPT a. amount of physiological stress b. metabolic demands of exercise c. type of physiological stress d. energy expended 2. Which of the following hormones enhance(s) muscle tissue growth? I. growth hormone II. cortisol III. IGF-I IV. progesterone a. I and III only b. II and IV only c. I, II, and III only d. II, III, and IV only 3. Which of the following is NOT a function of growth hormone? a. increase lipolysis b. decrease collagen synthesis c. increase amino acid transport d. decrease glucose utilization 4. Which of the following hormones has the greatest influence on neural changes? a. growth hormone b. testosterone c. cortisol d. IGF 5. What type of resistance training workout promotes the highest growth hormone increases following the exercise session? Rest Volume Sets a. 30 seconds High 3 b. 30 seconds Low 1 c. 3 minutes High 1 d. 3 minutes Low 3 Key terms Study questions (NSCA) supports and disseminates research-based knowledge and its practical application to improve ath- letic performance and fitness. With over 30,000 members in more than 50 countries, the NSCA has established itself as an international clearinghouse for strength and conditioning research, theories, and practices.
The CSCS and NSCA-CPT were the first certifica-tions of their kind to be nationally accredited by the National Commission for Certifying Agencies, a non- governmental, nonprofit agency in Washington, DC, that sets national standards for certifying agencies. To date, more than 40,000 professionals residing in 75 countries hold one or more NSCA certifications.
Whether used for learning the essentials of strength training and conditioning, for preparing for a certifica- tion exam, or as a reference by professionals, Essentials of Strength Training and Conditioning, Fourth Edition, will help practitioners and the scientific community better understand how to develop and administer safe and effective strength training and conditioning programs. www.ebook3000.com
ACCESSING THE LAB ACTIVITIES The lab activities are accessed through the web resource.
Individuals who purchase a new print book will receive access to the web resource via a key code.
The web resource can be accessed at www.HumanKinetics.com/EssentialsOfStrengthTrainingAnd Conditioning. Following is a list of the lab activities. Lab 1: Anaerobic Capacity Testing 300-Yard (274 m) Shuttle Run Lab 2: Aerobic Capacity Testing 1.5-Mile (2.4 km) Run 12-Minute Run Lab 3: Anthropometry and Body Composition Skinfold Measurements Lab 4: Exercise Testing for Athletes Test Selection and Order Lab 5: Techniques of Exercise Flexibility Exercise Techniques Lab 6: Techniques of Exercise Resistance Exercise and Spotting Guidelines Lab 7: Muscular Strength and Power Testing Vertical Jump Test Standing Long Jump Test 1RM Bench Press 1RM Back Squat Lab 8: Techniques of Exercise Plyometric Exercise Techniques Lab 9: Speed and Agility Technique and Testing T-Test Hexagon Test Pro Agility Test 40-Yard (37 m) Sprint Lab 10: Muscular Endurance Testing Push-Up Test YMCA Bench Press Test Partial Curl-Up Test Lab 11: Facility Layout Design Facility Floor Plan
ACKNOWLEDGMENTS The development of the fourth edition of the NSCA’s Essentials of Strength Training and Conditioning was a massive undertaking that would not have been possible without the contributions of a vast number of people. The historic development of this iconic text has served as our guiding principle, and the hard work of the numerous authors who contributed to the three previous editions has established a strong foundation for this text. There- fore, we thank the previous editors, Thomas Baechle and Roger Earle, for their foresight over twenty years ago that has led us to where we are today and for their passionate work on all of the previous editions. This edi- tion would not have been possible without the continued contribution of Roger Earle, who has gone beyond his role as a Human Kinetics representative. He is a true friend who has helped with many aspects of this book and our writing careers.
We would also like to thank Keith Cinea and Carwyn Sharp for their help throughout the process. These indi- viduals have represented the NSCA well and positioned the science that underpins our profession as the standard that determines the content of this text. Because it is a key resource for current and future strength and condi- tioning professionals, it was essential for us to ensure that this text holds true to the NSCA mission of trans- lating science into practice, and both Keith and Carwyn are ambassadors of this philosophy. Thanks also to the multitude of individuals at Human Kinetics who were essential to completing every phase of the publication of this book, from copyediting to graphic design. Prob- ably the most important note of thanks goes to Chris Drews and Karla Walsh, our developmental editor and managing editor, who helped two novice book editors in countless ways. Without Chris and Karla, we would have probably been lost in the process. G. Gregory Haff, PhD, CSCS,*D, FNSCA To my coeditor and long-time friend, Travis Triplett: I could think of no one else I would want to edit a book of this magnitude with. Your kind heart and easygoing style is a perfect complement to my “bull in a china shop” methodology for processes like this. Thanks for always being one of my very best friends!
I have to thank my family. My wife Erin has sacrificed everything to allow me the ability to chase my dreams and undertake projects like this. Without her support I would merely be stuck under the heavy lifting bar of life. It is a blessing to have someone strong enough to spot you when times are tough, and for that I love you more than you know. For my father, Guy Haff—I doubt you ever thought that lifting weights would become my whole life’s work when you took me to the West Morris YMCA at 11 years of age to teach me to lift. With- out that I cannot imagine who I would be at this moment. Finally, I must dedicate my efforts to my mother, Sandra Haff. No matter where you are now, I hope you are still proud of the man I am and the man I strive to be each and every day. I miss you much, Mom, and I wish you were here to see all the great things that have happened. N. Travis Triplett, PhD, CSCS,*D, FNSCA I never dreamed that taking my first weight training class while at the university would have culminated in such a rewarding career in the field of strength and conditioning. It is difficult to thank every person who had a role in getting me to this point in my life and my career, which enabled me to enthusiastically embark on this project. I was fortunate to receive a strong foundation from my parents—I wish you could both be here to see that the example you set was followed. I also want to thank my brother and my circle of friends, who have always been supportive and have been there to brighten my day. Professionally, my two greatest influences have been Mike Stone and Bill Kraemer. I value your mentorship and friendship greatly. Numerous colleagues and former students around the world have contributed to my knowledge and success along the way, and I appreciate each and every one of you even if we don’t see each other very often.
Finally, to my co-editor and good friend, Greg Haff: Who would have thought that sitting around at the lunch buffet as graduate students talking strength and condi- tioning would have led to this? I look forward to many more years of friendship and collaboration.
CREDITS Figure 2.5 Reprinted, by permission, from B.A. Gowitzke and M. Milner, 1988. Scientific bases of human movement, 3rd ed. (Baltimore, MD: Lippincott, Williams & Wilkins), 184-185. Figure 2.10 Reprinted, by permission, from E.A. Harman, M. Johnson, and P.N. Frykman, 1992, “A movement-oriented approach to exercise prescription,” NSCA Journal 14 (1): 47-54. Figure 2.13 Reprinted from K. Jorgensen, 1976, “Force- velocity relationship in human elbow flexors and extensors.” In Biomechanics A-V, edited by P.V. Komi (Baltimore, MD: University Park Press), 147. By permission of P.V. Komi. Figure 4.5 Reprinted from Steroids, Vol. 74(13-14), J.L. Vingren, W.J. Kraemer, et al., “Effect of resistance exercise on muscle steroid receptor protein content in strength trained men and women,” pgs. 1033-1039, copyright 2009, with permission from Elsevier. Figure 4.7 Adapted from W.J. Kraemer et al., 1998, “Hor- monal responses to consecutive days of heavy-resistance exer- cise with or without nutritional supplementation,” Journal of Applied Physiology 85 (4): 1544-1555. Used with permission. Table 5.3 Reprinted, by permission, from A. Fry, 1993, “Physiological responses to short-term high intensity resis- tance exercise overtraining,” Ph.D. Diss., The Pennsylvania State University; Meeusen R, Duclos M, Foster C, Fry A, Gleeson et al., 2013, “Prevention, diagnosis, and treatment of the over training syndrome: joint consensus statement of the European College of Sports Science and the American College of Sports Medicine,” Medicine and Science in Sport and Exercise 45: 186-205. Figure 7.2 Reprinted, by permission, from A.D. Faigen- baum et al., 2013, “Youth resistance training: past practices, new perspectives and future directions,” Pediatric Exercise Science 25: 591-604. Figure 7.3a © Hossler, PhD/Custom Medical Stock Photo— All rights reserved. Figure 7.3b © SPL/Custom Medical Stock Photo—All rights reserved. Figure 8.1 Reprinted, by permission, from R.S. Weinberg and D. Gould, 2015, Foundations of sport and exercise psy- chology, 6th ed. (Champaign, IL: Human Kinetics), 79. Figure 8.2 Reprinted, by permission, from B.D. Hatfield and G.A. Walford, 1987, “Understanding anxiety: Implications for sport performance,” NSCA Journal 9(2): 60-61. Table 9.6 Adapted, by permission, from K. Foster-Powell, S. Holt, and J.C. Brand-Miller, 2002, “International table of gly- cemic index and glycemic load values,” American Journal of Clinical Nutrition 76: 5-56. © American Society for Nutrition. Table 9.10 Reprinted, by permission, from M.N. Sawka et al., 2007, “American College of Sports Medicine position stand. Exercise and fluid replacement,” Medicine and Science of Sport and Exercise 39: 377-390, 2007. Table 10.5 Reprinted, by permission, from National Heart, Lung, and Blood Institute, 1998, “Clinical guidelines on the identification, evaluation, and treatment of overweight and obesity in adults: The evidence report,” Obesity Research 6: 464. Table 10.6 Reprinted, by permission, from National Heart, Lung, and Blood Institute, 1998, “Clinical guidelines on the identification, evaluation, and treatment of overweight and obesity in adults: The evidence report,” Obesity Research 6: 464. Figure 13.6 Adapted, by permission, from G.M. Gilliam, 1983, “300 yard shuttle run,” NSCA Journal 5 (5): 46. Figure 13.11 Adapted, by permission, from D. Semenick, 1990, “Tests and measurements: The T-test,” NSCA Journal 12(1): 36-37. Figure 13.12 Adapted, by permission, from K. Pauole et al., 2000, “Reliability and validity of the T-test as a measure of agility, leg power, and leg speed in college age males and females,” Journal of Strength and Conditioning Research 14: 443-450. Figure 13.16 Reprinted, by permission, from M.P. Reiman, 2009, Functional testing in performance (Champaign, IL: Human Kinetics), 109. Table 13.1 Adapted, by permission, from J. Hoffman, 2006, Norms for fitness, performance, and health (Champaign, IL: Human Kinetics), 36-37. Table 13.2 Reprinted, by permission, from J. Hoffman, 2006, Norms for fitness, performance, and health (Champaign, IL: Human Kinetics), 36-37. Table 13.3 Reprinted, by permission, from J. Hoffman, 2006, Norms for fitness, performance, and health (Champaign, IL: Human Kinetics), 38. Table 13.5 Reprinted, by permission, from J. Hoffman, 2006, Norms for fitness, performance, and health (Champaign, IL: Human Kinetics), 58. Adapted from D.A. Chu, 1996, Explosive power and strength (Champaign, IL: Human Kinetics). Table 13.6 Reprinted, by permission, from J. Hoffman, 2006, Norms for fitness, performance, and health (Champaign, IL: Human Kinetics), 58; adapted from D.A. Chu, 1996, Explosive power and strength (Champaign, IL: Human Kinetics).
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CHAPTER 1 Structure and Function of Body Systems N. Travis Triplett, PhD The author would like to acknowledge the significant contributions of Robert T. Harris and Gary R. Hunter to this chapter. After completing this chapter, you will be able to • describe both the macrostructure and microstructure of muscle and bone, • describe the sliding-filament theory of muscular contraction, • describe the specific morphological and physiological characteristics of different muscle fiber types and predict their relative involvement in different sport events, and • describe the anatomical and physiological characteristics of the cardiovascular and respiratory systems.
Physical exercise and sport performance involve effective, purposeful movements of the body. These movements result from the forces developed in muscles, which move the various body parts by acting through lever systems of the skeleton. These skeletal muscles are under the control of the cerebral cortex, which activates the skeletal muscle cells or fibers through the motor neurons of the peripheral nervous system. Support for this neuromuscular activity involves continuous delivery of oxygen and nutrients to working tissues and removal of carbon dioxide and metabolic waste by-products from working tissues through activities of the cardiovascular and respiratory systems.
In order to best apply the available scientific knowl-edge to the training of athletes and the development of effective training programs, strength and conditioning professionals must have a basic understanding of not only musculoskeletal function but also those systems of the body that directly support the work of exercising muscle. Accordingly, this chapter summarizes those aspects of the anatomy and function of the musculo- skeletal, neuromuscular, cardiovascular, and respiratory systems that are essential for developing and maintaining muscular force and power.
The musculoskeletal system of the human body consists of bones, joints, muscles, and tendons configured to allow the great variety of movements characteristic of human activity. This section describes the various com- ponents of the musculoskeletal system, both individually and in the context of how they function together.
The muscles of the body do not act directly to exert force on the ground or other objects. Instead, they function by pulling against bones that rotate about joints and transmit force to the environment. Muscles can only pull, not push; but through the system of bony levers, muscle pulling forces can be manifested as either pulling or pushing forces against external objects.
There are approximately 206 bones in the body, though the number can vary. This relatively light, strong structure provides leverage, support, and protection (figure 1.1). The axial skeleton consists of the skull (cranium), vertebral column (vertebra C1 through the coccyx), ribs, and sternum. The appendicular skele- ton includes the shoulder (or pectoral) girdle (left and right scapula and clavicle); bones of the arms, wrists, and hands (left and right humerus, radius, ulna, carpals, metacarpals, and phalanges); the pelvic girdle (left and right coxal or innominate bones); and the bones of the legs, ankles, and feet (left and right femur, patella, tibia, fibula, tarsals, metatarsals, and phalanges).
Junctions of bones are called joints. Fibrous joints (e.g., sutures of the skull) allow virtually no movement; cartilaginous joints (e.g., intervertebral disks) allow limited movement; and synovial joints (e.g., elbow and knee) allow considerable movement. Sport and exercise movements occur mainly about the synovial joints, whose most important features are low friction and large range of motion. Articulating bone ends are covered with smooth hyaline cartilage, and the entire joint is enclosed in a capsule filled with synovial fluid. There are usually additional supporting structures of ligament and cartilage (13).
Virtually all joint movement consists of rotation about points or axes. Joints can be categorized by the number of directions about which rotation can occur. Uniaxial joints, such as the elbow, operate as hinges, essentially rotating about only one axis. The knee is often referred to as a hinge joint, but its axis of rotation actually changes throughout the joint range of motion. Biaxial joints, such as the ankle and wrist, allow movement about two perpendicular axes. Multiaxial joints, including the shoulder and hip ball-and-socket joints, allow movement about all three perpendicular axes that define space.
The vertebral column is made up of vertebral bones separated by flexible disks that allow movement to occur. The vertebrae are grouped into 7 cervical vertebrae in the neck region; 12 thoracic vertebrae in the middle to upper back; 5 lumbar vertebrae, which make up the lower back; 5 sacral vertebrae, which are fused together and
There are several things that can positively affect the adult skeleton, and most are a result of muscle use.
When the body is subjected to heavy loads (job tasks or resistance training), the bone will increase in density
and bone mineral content. If the body performs more explosive movements with impact, similar changes
can occur. Some of the higher bone densities have been seen in people who engage in gymnastics or other
activities that involve high-strength and high-power movements, some with hard landings (11). Other factors
that influence bone adaptations are whether the axial skeleton is loaded and how often this loading occurs
(frequency). Since the adaptation period of bone is longer than that of skeletal muscle, it is important to vary
the stimulus in terms of frequency, intensity, and type.
a b Clavicle Sternum Humerus Ribs Pelvis Scapula Crest of pelvis (iliac crest) Vertebral column Radius Ulna Femur Tibia Patella Fibula Metacarpals Carpals Metatarsals E6372/NSCA/fig01.01/508626/alw/r1-pulled make up the rear part of the pelvis; and 3 to 5 coccygeal vertebrae, which form a kind of vestigial internal tail extending downward from the pelvis.
The system of muscles that enables the skeleton to move is depicted in figure 1.2. The connection point between bones is the joint, and skeletal muscles are attached to bones at each of their ends. Without this arrangement, movement could not occur.
Each skeletal muscle is an organ that contains muscle tissue, connective tissue, nerves, and blood vessels.
Fibrous connective tissue, or epimysium, covers the body’s more than 430 skeletal muscles. The epimysium is contiguous with the tendons at the ends of the muscle (figure 1.3). The tendon is attached to bone periosteum, a specialized connective tissue covering all bones; any contraction of the muscle pulls on the tendon and, in turn, the bone. Limb muscles have two attachments to bone: proximal (closer to the trunk) and distal (farther from the trunk). The two attachments of trunk muscles are termed superior (closer to the head) and inferior (closer to the feet).
Muscle cells, often called muscle fibers, are long (sometimes running the entire length of a muscle), cylin- drical cells 50 to 100 µm in diameter (about the diameter of a human hair). These fibers have many nuclei situated on the periphery of the cell and have a striated appearance
Deltoid Adductor longus Gracilis Sartorius Brachioradialis Brachialis External oblique Finger flexors Vastus medialis Rectus femoris Pectoralis major Biceps brachii Rectus abdominis Vastus lateralis Tibialis anterior a E6372/NSCA/fig01.02a/508073/alw/r1-pulled Trapezius Infraspinatus Teres major Triceps brachii Latissimus dorsi Finger extensors Gluteus maximus Semitendinosus Biceps femoris Semimembranosus Gastrocnemius Soleus b E6372/NSCA/fig01.02b/508074/alw/r1-pulled
Tendon Sarcoplasm Myofibril Perimysium Fasciculus Muscle belly Epimysium (deep fascia) Endomysium (between fibers) Nucleus Sarcolemma Single muscle fiber Myofilaments actin (thin) myosin (thick) E6372/NSCA/fig01.03/508017/alw/r1-pulled
perimysium (surrounding each fasciculus, or group of fibers), and endomysium (surrounding individual fibers). www.ebook3000.com
under low magnification. Under the epimysium the muscle fibers are grouped in bundles (fasciculi) that may consist of up to 150 fibers, with the bundles sur- rounded by connective tissue called perimysium. Each muscle fiber is surrounded by connective tissue called endomysium, which is encircled by and is contiguous with the fiber’s membrane, or sarcolemma (13). All the connective tissue—epimysium, perimysium, and endomysium—is contiguous with the tendon, so tension developed in a muscle cell is transmitted to the tendon and the bone to which it is attached (see figure 1.3).
The junction between a motor neuron (nerve cell) and the muscle fibers it innervates is called the motor end plate, or, more often, the neuromuscular junction (figure 1.4). Each muscle cell has only one neuromuscu- lar junction, although a single motor neuron innervates many muscle fibers, sometimes hundreds or even thou- sands. A motor neuron and the muscle fibers it innervates are called a motor unit. All the muscle fibers of a motor unit contract together when they are stimulated by the motor neuron.
The interior structure of a muscle fiber is depicted in figure 1.5. The sarcoplasm, which is the cytoplasm of a muscle fiber, contains contractile components consisting of protein filaments, other proteins, stored glycogen and fat particles, enzymes, and specialized organelles such as mitochondria and the sarcoplasmic reticulum.
Hundreds of myofibrils (each about 1 mm in diam-eter, 1/100 the diameter of a hair) dominate the sarco- plasm. Myofibrils contain the apparatus that contracts the muscle cell, which consists primarily of two types of myofilament: myosin and actin. The myosin fila- ments (thick filaments about 16 nm in diameter, about 1/10,000 the diameter of a hair) contain up to 200 myosin molecules. The myosin filament consists of a globular head, a hinge point, and a fibrous tail. The globular heads protrude away from the myosin filament at regular intervals, and a pair of myosin filaments forms a cross- bridge, which interacts with actin. The actin filaments (thin filaments about 6 nm in diameter) consist of two strands arranged in a double helix. Myosin and actin filaments are organized longitudinally in the smallest contractile unit of skeletal muscle, the sarcomere. Sarco- meres average about 2.5 mm in length in a relaxed fiber (approximately 4,500 per centimeter of muscle length) and are repeated the entire length of the muscle fiber (1).
Figure 1.6 shows the structure and orientation of the myosin and actin in the sarcomere. Adjacent myosin filaments anchor to each other at the M-bridge in the center of the sarcomere (the center of the H-zone). Actin filaments are aligned at both ends of the sarcomere and are anchored at the Z-line. Z-lines are repeated through the entire myofibril. Six actin filaments surround each myosin filament, and each actin filament is surrounded by three myosin filaments.
It is the arrangement of the myosin and actin fil-aments and the Z-lines of the sarcomeres that gives skeletal muscle its alternating dark and light pattern, which appears as striated under magnification. The dark A-band corresponds with the alignment of the myosin Nucleus Axon Neuromuscular junction Muscle Node of Ranvier Dendrites Myelin sheath Nucleus Axon Neuromuscular junction Muscle Node of Ranvier Dendrites Myelin sheath E6372/NSCA/fig01.04/508018/alw/r1-pulled
and the muscle fibers it innervates. There are typically several hundred muscle fibers in a single motor unit. Myofibril Mitochondrion T-tubule Opening to T-tubule Sarcolemma Sarcoplasmic reticulum E6372/NSCA/fig01.05/508019/alw/r1-pulled
Sarcomere Z-line Z-line end H-zone I-band A-band M-line H-zone level Myofibril Myosin (thick) filament Backbone Resting state Head Actin (thin) filament Actin Actin Troponin Tropomyosin Z-line M-line M-bridge A-bandI-band Actin filament Myosin filament Myofilaments (cross sections) Myosin Cross-bridge Tail E6372/NSCA/fig01.06/508020/alw/r1-pulled
and actin (thin) filaments gives skeletal muscle its striated appearance. filaments, whereas the light I-band corresponds with the areas in two adjacent sarcomeres that contain only actin filaments (13). The Z-line is in the middle of the I-band and appears as a thin, dark line running longitudinally through the I-band. The H-zone is the area in the center of the sarcomere where only myosin filaments are pres- ent. During muscle contraction, the H-zone decreases as the actin slides over the myosin toward the center of the sarcomere. The I-band also decreases as the Z-lines are pulled toward the center of the sarcomere.
Parallel to and surrounding each myofibril is an intricate system of tubules, called the sarcoplasmic reticulum (see figure 1.5), which terminates as vesicles in the vicinity of the Z-lines. Calcium ions are stored in the vesicles. The regulation of calcium controls mus- cular contraction. T-tubules, or transverse tubules, run
perpendicular to the sarcoplasmic reticulum and termi- nate in the vicinity of the Z-line between two vesicles. Because the T-tubules run between outlying myofibrils and are contiguous with the sarcolemma at the surface of the cell, discharge of an action potential (an electrical nerve impulse) arrives nearly simultaneously from the surface to all depths of the muscle fiber. Calcium is thus released throughout the muscle, producing a coordinated contraction. ▶ The discharge of an action potential from a motor nerve signals the release of calcium from the sarcoplasmic reticulum into the myofibril, causing tension development in muscle.
In its simplest form, the sliding-filament theory states that the actin filaments at each end of the sarcomere slide inward on myosin filaments, pulling the Z-lines toward the center of the sarcomere and thus shortening the muscle fiber (figure 1.7). As actin filaments slide over myosin filaments, both the H-zone and I-band shrink. The action of myosin crossbridges pulling on the actin filaments is responsible for the movement of the actin filament. Because only a very small displacement of the actin filament occurs with each flexion of the myosin crossbridge, very rapid, repeated flexions must occur in many crossbridges throughout the entire muscle for measurable movement to occur (13).
calcium is present in the myofibril (most of it is stored in the sarcoplasmic reticulum), so very few of the myosin crossbridges are bound to actin. Even with the actin binding site covered, myosin and actin still interact in a weak bond, which becomes strong (and muscle tension is produced) when the actin binding site is exposed after release of the stored calcium.
myosin crossbridges can flex, they must first attach to the actin filament. When the sarcoplasmic reticulum is stimulated to release calcium ions, the calcium binds with troponin, a protein that is situated at regular inter- vals along the actin filament (see figure 1.6) and has a high affinity for calcium ions. This causes a shift to occur in another protein molecule, tropomyosin, which runs along the length of the actin filament in the groove of the A-band I-bandI-band Z-line H-zone Z-line a Myosin filament Actin filament E6372/NSCA/fig01.07a/508021/alw/r1-pulled A-band I-bandI-band Z-line H-zone Z-line b E6372/NSCA/fig01.07b/513635/alw/r1-pulled A-band Z-lineZ-line c E6372/NSCA/fig01.07c/513636/alw/r1-pulled
force potential due to reduced crossbridge–actin alignment. (b) When muscle contracts (here partially), the I-bands and H-zone are shortened. Force potential is high due to optimal crossbridge–actin alignment. (c) With contracted muscle, force potential is low because the overlap of actin reduces the potential for crossbridge–actin alignment.
double helix. The myosin crossbridge now attaches much more rapidly to the actin filament, allowing force to be produced as the actin filaments are pulled toward the center of the sarcomere (1). It is important to understand that the amount of force produced by a muscle at any instant in time is directly related to the number of myosin crossbridges bound to actin filaments cross-sectionally at that instant in time (1). ▶ The number of crossbridges that are formed between actin and myosin at any instant in time dictates the force production of a muscle.
or power stroke, comes from hydrolysis (breakdown) of adenosine triphosphate (ATP) to adenosine diphos- phate (ADP) and phosphate, a reaction catalyzed by the enzyme myosin adenosine triphosphatase (ATPase). Another molecule of ATP must replace the ADP on the myosin crossbridge globular head in order for the head to detach from the active actin site and return to its original position. This allows the contraction process to continue (if calcium is available to bind to troponin) or relaxation to occur (if calcium is not available). It may be noted that calcium plays a role in regulating a large number of events in skeletal muscle besides contraction. These include glycolytic and oxidative energy metabolism, as well as protein synthesis and degradation (10). ▶ Calcium and ATP are necessary for cross- bridge cycling with actin and myosin fila- ments.
transpires only when this sequence of events—binding of calcium to troponin, coupling of the myosin cross- bridge with actin, power stroke, dissociation of actin and myosin, and resetting of the myosin head position—is repeated over and over again throughout the muscle fiber. This occurs as long as calcium is available in the myofibril, ATP is available to assist in uncoupling the myosin from the actin, and sufficient active myosin ATPase is available for catalyzing the breakdown of ATP.
ulation of the motor nerve stops. Calcium is pumped back into the sarcoplasmic reticulum, which prevents the link between the actin and myosin filaments. Relaxation is brought about by the return of the actin and myosin filaments to their unbound state.
Muscle fibers are innervated by motor neurons that trans- mit impulses in the form of electrochemical signals from the spinal cord to muscle. A motor neuron generally has numerous terminal branches at the end of its axon and thus innervates many different muscle fibers. The whole structure is what determines the muscle fiber type and its characteristics, function, and involvement in exercise.
When a motor neuron fires an impulse or action poten- tial, all of the fibers that it serves are simultaneously activated and develop force. The extent of control of a muscle depends on the number of muscle fibers within each motor unit. Muscles that must function with great precision, such as eye muscles, may have motor units with as few as one muscle fiber per motor neuron. Changes in the number of active motor units in these small muscles can produce the extremely fine gradations in force that are necessary for precise movements of the eyeball. In contrast, the quadriceps muscle group, which moves the leg with much less precision, may have sev- eral hundred fibers served by one motor neuron.
The steps of muscle contraction can be summarized as follows:1. Initiation of ATP splitting (by myosin ATPase) causes myosin head to be in an “energized” state that allows it to move into a position to be able to form a bond with actin. 2. The release of phosphate from the ATP splitting process then causes the myosin head to change shape and shift. 3. This pulls the actin lament in toward the center of the sarcomere and is referred to as the power stroke; ADP is then released. 4. Once the power stroke has occurred, the myosin head detaches from the actin but only after another ATP binds to the myosin head because the binding process facilitates detachment. 5. The myosin head is now ready to bind to another actin (as described in step 1), and the cycle contin- ues as long as ATP and ATPase are present and calcium is bound to the troponin.
The action potential (electric current) that flows along a motor neuron is not capable of directly exciting muscle fibers. Instead, the motor neuron excites the muscle fiber(s) that it innervates by chemical transmis- sion. Arrival of the action potential at the nerve terminal causes release of a neurotransmitter, acetylcholine, which diffuses across the neuromuscular junction, causing excitation of the sarcolemma. Once a sufficient amount of acetylcholine is released, an action potential is generated along the sarcolemma, and the fiber contracts. All of the muscle fibers in the motor unit contract and develop force at the same time. There is no evidence that a motor neuron stimulus causes only some of the fibers to contract. Similarly, a stronger action potential cannot produce a stronger contraction. This phenomenon is known as the all-or-none principle of muscle.
Each action potential traveling down a motor neuron results in a short period of activation of the muscle fibers within the motor unit. The brief contraction that results is referred to as a twitch. Activation of the sarcolemma results in the release of calcium within the fiber, and contraction proceeds as previously described. Force develops if there is resistance to the pulling interaction of actin and myosin filaments. Although calcium release during a twitch is sufficient to allow optimal activation of actin and myosin, and thereby maximal force of the fibers, calcium is removed before force reaches its max- imum, and the muscle relaxes (figure 1.8a). If a second twitch is elicited from the motor nerve before the fibers completely relax, force from the two twitches summates, and the resulting force is greater than that produced by a single twitch (figure 1.8b). Decreasing the time inter- val between the twitches results in greater summation of crossbridge binding and force. The stimuli may be delivered at so high a frequency that the twitches begin to merge and eventually completely fuse, a condition called tetanus (figure 1.8, c and d). This is the maximal amount of force the motor unit can develop.
Skeletal muscles are composed of fibers that have markedly different morphological and physiological characteristics. These differences have led to several different systems of classification, based on a variety of criteria. The most familiar approach is to classify fibers according to twitch time, employing the terms slow- twitch and fast-twitch fiber. Because a motor unit is composed of muscle fibers that are all of the same type, it also can be designated using this classification system. A fast-twitch motor unit is one that develops force and also relaxes rapidly and thus has a short twitch time. Slow-twitch motor units, in contrast, develop force and relax slowly and have a long twitch time.
Histochemical staining for myosin ATPase content is often used to classify fibers as slow-twitch or fast- twitch. Although the techniques can stain for multiple fiber types, the commonly identified fibers are Type I (slow-twitch), Type IIa (fast-twitch), and Type IIx (fast- twitch). Another more specific method is to quantify the amount of myosin heavy chain (MHC) protein; the nomenclature for this is similar to that with the myosin ATPase methodology.
The contrast in mechanical characteristics of Type I and Type II fibers is accompanied by a distinct difference in the ability of the fibers to demand and supply energy for contraction and thus to withstand fatigue. Type I fibers are generally efficient and fatigue resistant and have a high capacity for aerobic energy supply, but they have limited potential for rapid force development, as characterized by low myosin ATPase activity and low anaerobic power (2, 8).
Type II motor units are essentially the opposite, char-acterized as inefficient and fatigable and as having low aerobic power, rapid force development, high myosin ATPase activity, and high anaerobic power (2, 8). Type IIa and Type IIx fibers differ mainly in their capacity for aerobic–oxidative energy supply. Type IIa fibers, for example, have greater capacity for aerobic metabolism and more capillaries surrounding them than Type IIx and therefore show greater resistance to fatigue (3, 7, 9, 12). Based on these differences, it is not surprising that postural muscles, such as the soleus, have a high composition of Type I fibers, whereas large, so-called locomotor muscles, such as the quadriceps group, have a mixture of both Type I and Type II fibers to enable both low and high power output activities (such as jogging and sprinting, respectively). Refer to table 1.1 for a summary of the primary characteristics of fiber types. Frequency Force a b c d E6372/NSCA/fig01.08/508022/alw/r1-pulled
motor unit: a = single twitch; b = force resulting from summation of two twitches; c = unfused tetanus; d = fused tetanus.
▶ Motor units are composed of muscle fibers with specific morphological and physio- logical characteristics that determine their functional capacity.
Through everyday experiences, we are quite aware that a given muscle can vary its level of force output according to the level required by a particular task. This ability to vary or gradate force is essential for performance of smooth, coordinated patterns of movement. Muscular force can be graded in two ways. One is through varia- tion in the frequency at which motor units are activated. If a motor unit is activated once, the twitch that arises does not produce a great deal of force. However, if the frequency of activation is increased so that the forces of the twitches begin to overlap or summate, the resulting force developed by the motor unit is much greater. This method of varying force output is especially important in small muscles, such as those of the hand. Even at low forces, most of the motor units in these muscles are activated, albeit at a low frequency. Force output of the whole muscle is intensified through increase in the frequency of firing of the individual motor units. The other means of varying skeletal muscle force involves an increase in force through varying the number of motor units activated, a process known as recruitment. In large muscles, such as those in the thigh, motor units are activated at near-tetanic frequency when called on. Increases in force output are achieved through recruit- ment of additional motor units.
The type of motor unit recruited for a given activity is determined by its physiological characteristics (table 1.2). For an activity such as distance running, slow- twitch motor units are engaged to take advantage of their remarkable efficiency, endurance capacity, and resistance to fatigue. If additional force is needed, as in a sprint at the end of a race, the fast-twitch motor units are called into play to increase the pace; unfortunately, exercise at such intensity cannot be maintained very long. If the activity requires near-maximal performance, as in a power clean, most of the motor units are called into play, with fast-twitch units making the more signif- icant contribution to the effort. Complete activation of the available motor neuron pool is probably not possible in untrained people (4, 5, 6). Although the large fast- twitch units may be recruited if the effort is substantial, under most circumstances it is probably not possible to activate them at a high enough frequency for maximal force to be realized.
CharacteristicFiber types Type I Type IIa Type IIx Motor neuron size Small Large Large Recruitment threshold Low Intermediate/High High Nerve conduction velocity Slow Fast Fast Contraction speed Slow Fast Fast Relaxation speed Slow Fast Fast Fatigue resistance High Intermediate/Low Low Endurance High Intermediate/Low Low Force production Low Intermediate High Power output Low Intermediate/High High Aerobic enzyme content High Intermediate/Low Low Anaerobic enzyme content Low High High Sarcoplasmic reticulum complexity Low Intermediate/High High Capillary density High Intermediate Low Myoglobin content High Low Low Mitochondrial size, density High Intermediate Low Fiber diameter Small Intermediate Large Color Red White/Red White
Sensory neuron Motor neuron Intrafusal fiber Extrafusal fiber Muscle spindle E6372/NSCA/fig01.09/508026/alw/r1-pulled ▶ The force output of a muscle can be varied through change in the frequency of activa- tion of individual motor units or change in the number of activated motor units.
Proprioceptors are specialized sensory receptors located within joints, muscles, and tendons. Because these receptors are sensitive to pressure and tension, they relay information concerning muscle dynamics to the conscious and subconscious parts of the central nervous system. The brain is thus provided with information con- cerning kinesthetic sense, or conscious appreciation of the position of body parts with respect to gravity. Most of this proprioceptive information, however, is processed at subconscious levels so we do not have to dedicate conscious activity toward tasks such as maintaining posture or position of body parts.
Event Type I Type II 100 m sprint Low High 800 m run High High Marathon High Low Olympic weightlifting Low High Soccer, lacrosse, hockey High High American football wide receiver Low High American football lineman Low High Basketball, team handball Low High Volleyball Low High Baseball or softball pitcher Low High Boxing High High Wrestling High High 50 m swim Low High Field events Low High Cross-country skiing, biathlon High Low Tennis High High Downhill or slalom skiing High High Speed skating High High Track cycling Low High Distance cycling High Low Rowing High High ▶ Proprioceptors are specialized sensory receptors that provide the central nervous system with information needed to maintain muscle tone and perform complex coordi- nated movements.
Muscle spindles are proprioceptors that consist of several modified muscle fibers enclosed in a sheath of connective tissue (figure 1.9). These modified fibers, called intrafusal fibers, run parallel to the normal, or extrafusal, fibers. Muscle spindles provide informa- tion concerning muscle length and the rate of change in length. When the muscle lengthens, spindles are stretched. This deformation activates the sensory neuron of the spindle, which sends an impulse to the spinal cord, where it synapses (connects) with motor neurons. This results in the activation of motor neurons that innervate the same muscle. Spindles thus indicate the degree to which the muscle must be activated in order to overcome a given resistance. As a load increases, the muscle is stretched to a greater extent, and engagement of muscle spindles results in greater activation of the muscle. Muscles that perform precise movements have many spindles per unit of mass to help ensure exact control of their contractile activity. A simple example of muscle spindle activity is the knee jerk reflex. Tapping on the tendon of the knee extensor muscle group below the patella stretches the muscle spindle fibers. This causes activation of extrafusal muscle fibers in the same muscle.
deformation of the muscle spindle activates the sensory neuron, which sends an impulse to the spinal cord, where it synapses with a motor neuron, causing the muscle to contract.
A knee jerk occurs as these fibers actively shorten. This, in turn, shortens the intrafusal fibers and causes their discharge to cease.
Golgi tendon organs (GTOs) are proprioceptors located in tendons near the myotendinous junction and are in series, that is, attached end to end, with extrafusal muscle fibers (figure 1.10). Golgi tendon organs are activated when the tendon attached to an active muscle is stretched. As tension in the muscle increases, discharge of the GTOs increases. The sensory neuron of the GTO synapses with an inhibitory interneuron in the spinal cord, which in turn synapses with and inhibits a motor neuron that serves the same muscle. The result is a reduction in tension within the muscle and tendon. Thus, whereas spindles facilitate activation of the muscle, neural input from GTOs inhibits muscle activation. The GTOs’ inhibitory process is thought to provide a mechanism that protects against the development of excessive tension. The effect of GTOs is therefore min- imal at low forces; but when an extremely heavy load is placed on the muscle, reflexive inhibition mediated by the GTOs causes the muscle to relax. The ability of the motor cortex to override this inhibition may be one of the fundamental adaptations to heavy resistance training.
The primary roles of the cardiovascular system are to transport nutrients and remove waste and by-products while assisting with maintaining the environment for all the body’s functions. The cardiovascular system plays key roles in the regulation of the body’s acid–base system, fluids, and temperature, as well as a variety of other physiological functions. This section describes the anatomy and physiology of the heart and the blood vessels.
The heart is a muscular organ composed of two inter- connected but separate pumps; the right side of the heart pumps blood through the lungs, and the left side pumps blood through the rest of the body. Each pump has two chambers: an atrium and a ventricle (figure 1.11). The right and left atria deliver blood into the right and left ventricles. The right and left ventricles supply the main force for moving blood through the pulmonary and peripheral circulations, respectively (13).
The tricuspid valve and mitral valve (bicuspid valve) (collectively called atrioventricular [AV] valves) pre- vent the flow of blood from the ventricles back into the atria during ventricular contraction (systole). The aortic valve and pulmonary valve (collectively, the semilunar valves) prevent backflow from the aorta and pulmonary arteries into the ventricles during ventricular relaxation (diastole). Each valve opens and closes passively; that is, each closes when a backward pressure gradient pushes blood back against it, opening when a forward pressure gradient forces blood in the forward direction (13).
• Incorporate phases of training that use heavier loads in order to optimize neural recruitment. • Increase the cross-sectional area of muscles involved in the desired activity. • Perform multimuscle, multijoint exercises that can be done with more explosive actions to optimize fast-twitch muscle recruitment. Sensory neuron Motor neuron Inhibitory interneuron Muscle Tendon Golgi tendon organ E6372/NSCA/fig01.10/508027/alw/r1-pulled
extremely heavy load is placed on the muscle, discharge of the GTO occurs. The sensory neuron of the GTO activates an inhibitory interneuron in the spinal cord, which in turn synapses with and inhibits a motor neuron serving the same muscle.
A specialized electrical conduction system (figure 1.12) controls the mechanical contraction of the heart. The conduction system is composed of • the sinoatrial (SA) node—the intrinsic pace- maker—where rhythmic electrical impulses are normally initiated; • the internodal pathways that conduct the impulse from the SA node to the atrioventricular node; • the atrioventricular (AV) node, where the impulse is delayed slightly before passing into the ventricles; • the atrioventricular (AV) bundle, which con- ducts the impulse to the ventricles; and • the left bundle branch and right bundle branch, which further divide into the Purkinje fibers and conduct impulses to all parts of the ventricles.
The SA node is a small area of specialized muscle tissue located in the upper lateral wall of the right atrium. The fibers of the node are contiguous with the muscle fibers of the atrium, with the result that each electrical impulse that begins in the SA node normally spreads immediately into the atria. The conductive system is organized so that the impulse does not travel into the ven- tricles too rapidly, allowing time for the atria to contract and empty blood into the ventricles before ventricular contraction begins. It is primarily the AV node and its associated conductive fibers that delay each impulse entering into the ventricles. The AV node is located in the posterior septal wall of the right atrium (13).
The left and right bundle branches lead from the AV bundle into the ventricles. Except for their initial portion, where they penetrate the AV barrier, these conduction fibers have functional characteristics quite opposite those of the AV nodal fibers. They are large and transmit impulses at a much higher velocity than the AV nodal fibers. Because these fibers give way to the Purkinje fibers, which more completely penetrate the ventricles, the impulse travels quickly throughout the entire ven- tricular system and causes both ventricles to contract at approximately the same time (13).
Trunk and lower extremity Head and upper extremity Aorta Pulmonary artery From left lung To left lung To right lung Left atrium Mitral valve Left ventricle Right ventricle Superior vena cava Inferior vena cava
Tricuspid valvePulmonary veins Pulmonary valve From right lung Right atrium Aortic valve E6372/NSCA/fig01.11/508028/alw/r1-pulled
The SA node normally controls heart rhythmicity because its discharge rate is considerably greater (60-80 times per minute) than that of either the AV node (40-60 times per minute) or the ventricular fibers (15-40 times per minute). Each time the SA node discharges, its impulse is conducted into the AV node and the ventricu- lar fibers, discharging their excitable membranes. Thus, these potentially self-excitatory tissues are discharged before self-excitation can actually occur.
The inherent rhythmicity and conduction properties of the myocardium (heart muscle) are influenced by the cardiovascular center of the medulla, which trans- mits signals to the heart through the sympathetic and parasympathetic nervous systems, both of which are components of the autonomic nervous system. The atria are supplied with a large number of both sympathetic and parasympathetic neurons, whereas the ventricles receive sympathetic fibers almost exclusively. Stimulation of the sympathetic nerves accelerates depolarization of the SA node (the chronotropic effect), which causes the heart to beat faster. Stimulation of the parasympathetic nervous system slows the rate of SA node discharge, which slows the heart rate. The resting heart rate normally ranges from 60 to 100 beats/min; fewer than 60 beats/min is called bradycardia, and more than 100 beats/min is called tachycardia.
The electrical activity of the heart can be recorded at the surface of the body; a graphic representation of this activity is called an electrocardiogram (ECG). A normal ECG, seen in figure 1.13, is composed of a P-wave, a QRS complex (the QRS complex is often three separate waves: a Q-wave, an R-wave, and an
heart. Millivolts 2 1 0 1 2 R S P P T Q E6372/NSCA/fig01.13/508031/alw/r2-pulled S-wave), and a T-wave. The P-wave and the QRS complex are recordings of electrical depolarization, that is, the electrical stimulus that leads to mechanical contraction. Depolarization is the reversal of the mem- brane electrical potential, whereby the normally negative potential inside the membrane becomes slightly positive and the outside becomes slightly negative. The P-wave is generated by the changes in the electrical potential of cardiac muscle cells that depolarize the atria and result in atrial contraction. The QRS complex is generated by the electrical potential that depolarizes the ventricles and results in ventricular contraction. In contrast, the T-wave is caused by the electrical potential generated as the ventricles recover from the state of depolarization; this process, called repolarization, occurs in ventricu- lar muscle shortly after depolarization. Although atrial repolarization occurs as well, its wave formation usually occurs during the time of ventricular depolarization and is thus masked by the QRS complex (13).
The central and peripheral circulation form a single closed-circuit system with two components: an arterial system, which carries blood away from the heart, and a venous system, which returns blood toward the heart (figure 1.14). The blood vessels of each system are identified here.
The function of arteries is to rapidly transport blood pumped from the heart. Because blood pumped from the heart is under relatively high pressure, arteries have strong, muscular walls. Small branches of arteries called arterioles act as control vessels through which blood enters the capillaries. Arterioles play a major role in the regulation of blood flow to the capillaries. Arterioles have strong, muscular walls that are capable of closing
SA node Internodal pathways Left bundle branch Right bundle branch AV node Purkinje fibers E6372/NSCA/fig01.12/508029/alw/r1-pulled
the arteriole completely or allowing it to be dilated many times their size, thus vastly altering blood flow to the capillaries in response to the needs of the tissues (13).
The function of capillaries is to facilitate exchange of oxygen, fluid, nutrients, electrolytes, hormones, and other substances between the blood and the interstitial fluid in the various tissues of the body. The capillary walls are very thin and are permeable to these, but not all, substances (13).
Venules collect blood from the capillaries and gradually converge into the progressively larger veins, which transport blood back to the heart. Because the pressure in the venous system is very low, venous walls are thin, although muscular. This allows them to constrict or dilate to a great degree and thereby act as a reservoir for blood, either in small or in large amounts (13). In addition, some veins, such as those in the legs, contain one-way valves that help maintain venous return by preventing retrograde blood flow. ▶ The cardiovascular system transports nutri- ents and removes waste products while helping to maintain the environment for all the body’s functions. The blood transports oxygen from the lungs to the tissues for use in cellular metabolism; and it transports carbon dioxide, the most abundant by-prod- uct of metabolism, from the tissues to the lungs, where it is removed from the body.
Two paramount functions of blood are the transport of oxygen from the lungs to the tissues for use in cellular metabolism and the removal of carbon dioxide, the most abundant by-product of metabolism, from the tissues to the lungs. The transport of oxygen is accomplished by hemoglobin, the iron–protein molecule carried by the red blood cells. Hemoglobin also has an additional important role as an acid–base buffer, a regulator of hydrogen ion concentration, which is crucial to the rates of chemical reactions in cells. Red blood cells, the major component of blood, have other functions as well. For instance, they contain a large quantity of carbonic anhydrase, which catalyzes the reaction between carbon dioxide and water to facilitate carbon dioxide removal.
The primary function of the respiratory system is the basic exchange of oxygen and carbon dioxide. The anat- omy of the human respiratory system is shown in figure 1.15. As air passes through the nose, the nasal cavities perform three distinct functions: warming, humidifying, and purifying the air (13). Air is distributed to the lungs by way of the trachea, bronchi, and bronchioles. The trachea is called the first-generation respiratory passage, and the right and left main bronchi are the second-gen- eration passages; each division thereafter is an additional generation (bronchioles). There are approximately 23 Pulmonary circulation: 9% Heart: 7% Arteries: 13% Veins, venules, and venous sinuses: 64% Arterioles and capillaries: 7% E6372/NSCA/fig01.14/508032/alw/r1-pulled
ponents of the circulatory system. The percent values indicate the distribution of blood volume throughout the circulatory system at rest.
The skeletal muscle pump is the assistance that contracting muscles provide to the circulatory system. The
muscle pump works with the venous system, which contains the one-way valves for blood return to the
heart. The contracting muscle compresses the veins, but since the blood can flow only in the direction of
the valves, it is returned to the heart. This mechanism is one of the reasons that individuals are told to keep
moving around after exercise to avoid blood pooling in the lower extremities. On the flip side, it is important
to periodically squeeze muscles during prolonged sitting to facilitate blood return to the heart.
E6372/Baechle/fig 01.15/508033/JanT/R1 Conchae Pharynx Glottis Esophagus Trachea Epiglottis Larynx, vocal cords Pulmonary artery Pulmonary vein Alveoli Bronchiole Right main bronchus Left main bronchus generations before the air finally reaches the alveoli, where gases are exchanged in respiration (13). ▶ The primary function of the respiratory system is the basic exchange of oxygen and carbon dioxide.
The amount and movement of air and expired gases in and out of the lungs are controlled by expansion and recoil of the lungs. The lungs do not actively expand and recoil themselves but rather are acted upon to do so in two ways: by downward and upward movement of the diaphragm to lengthen and shorten the chest cavity and by elevation and depression of the ribs to increase and decrease the back-to-front diameter of the chest cavity (13). Normal, quiet breathing is accomplished almost entirely by movement of the diaphragm. During inspi- ration, contraction of the diaphragm creates a negative pressure (vacuum) in the chest cavity, and air is drawn into the lungs. During expiration, the diaphragm simply relaxes; the elastic recoil of the lungs, chest wall, and abdominal structures compresses the lungs, and air is expelled. During heavy breathing, the elastic forces alone are not powerful enough to provide the necessary respiratory response. The extra required force is achieved mainly by contraction of the abdominal muscles, which push the abdomen upward against the bottom of the diaphragm (13).
The second method for expanding the lungs is to raise the rib cage. Because the chest cavity is small and the ribs are slanted downward while in the resting position, elevating the rib cage allows the ribs to project almost directly forward so that the sternum can move forward and away from the spine. The muscles that elevate the rib cage are called muscles of inspiration and include the external intercostals, the sternocleidomastoids, the anterior serrati, and the scaleni. The muscles that depress the chest are muscles of expiration and include the abdominal muscles (rectus abdominis, external and internal obliques, and transversus abdominis) and the internal intercostals (13).
Pleural pressure is the pressure in the narrow space between the lung pleura and the chest wall pleura (mem- branes enveloping the lungs and lining the chest walls). This pressure is normally slightly negative. Because the lung is an elastic structure, during normal inspiration the expansion of the chest cage is able to pull on the surface of the lungs and creates a more negative pressure, thus enhancing inspiration. During expiration, the events are essentially reversed (13).
Alveolar pressure is the pressure inside the alveoli when the glottis is open and no air is flowing into or out of the lungs. In fact, in this instance the pressure in all parts of the respiratory tree is the same all the way to the
alveoli and is equal to the atmospheric pressure. To cause inward flow of air during inspiration, the pressure in the alveoli must fall to a value slightly below atmospheric pressure. During expiration, alveolar pressure must rise above atmospheric pressure (13).
During normal respiration at rest, only 3% to 5% of the total energy expended by the body is required for pulmonary ventilation. During very heavy exercise, however, the amount of energy required can increase to as much as 8% to 15% of total body energy expenditure, especially if the person has any degree of increased airway resistance, as occurs with exercise-induced asthma. Precautions, including physician evaluation of the athlete, are often recommended, depending on the potential level of impairment.
With ventilation, oxygen diffuses from the alveoli into the pulmonary blood, and carbon dioxide diffuses from the blood into the alveoli. The process of diffusion is a simple random motion of molecules moving in opposite directions through the alveolar capillary membrane. The energy for diffusion is provided by the kinetic motion of the molecules themselves. Net diffusion of the gas occurs from the region of high concentration to the region of low concentration. The rates of diffusion of the two gases depend on their concentrations in the capillaries and alveoli and the partial pressure of each gas (13).
At rest, the partial pressure of oxygen in the alveoli is about 60 mmHg greater than that in the pulmonary capillaries. Thus, oxygen diffuses into the pulmonary capillary blood. Similarly, carbon dioxide diffuses in the opposite direction. This process of gas exchange is so rapid as to be thought of as instantaneous (13).
Knowledge of musculoskeletal, neuromuscular, car- diovascular, and respiratory anatomy and physiology is important for the strength and conditioning pro- fessional to have in order to understand the scientific basis for conditioning. This includes knowledge of the function of the macrostructure and microstructure of the skeleton and muscle fibers, muscle fiber types, and interactions between tendon and muscle and between the motor unit and its activation, as well as the interactions of the heart, vascular system, lungs, and respiratory system. This information is necessary for developing training strategies that will meet the specific needs of the athlete.
Regular exercise in general is beneficial for maintaining respiratory muscle function. Both endurance exercise,
which involves repetitive contraction of breathing muscles, and resistance exercise, which taxes the diaphragm
and abdominal muscles especially because of their use for stabilization and for increasing intra-abdominal
pressure (Valsalva maneuver) during exertion, can result in some muscle training adaptations. This can help
to preserve some of the pulmonary function with aging. However, it is generally not necessary to specifically
train the muscles of respiration except following surgery or during prolonged bed rest when the normal
breathing patterns are compromised.
A-band
acetylcholine
actin
action potential
all-or-none principle
alveolar pressure
alveoli
aortic valve
appendicular skeleton
arterial system
arteriole
artery
atrioventricular (AV) bundle
atrioventricular (AV) node
atrioventricular (AV) valvesatrium axial skeleton biaxial joints bone periosteum bradycardia bronchi bronchiole capillary cartilaginous joints crossbridge depolarization diastole diffusion distal electrocardiogram (ECG) endomysium epimysium extrafusal fibers fasciculi fast-twitch fiber fibrous joints Golgi tendon organ (GTO) hemoglobin hyaline cartilage H-zone I-band inferior intrafusal fibers left bundle branch mitral valve
motor neuron
motor unit
multiaxial joints
muscle fiber
muscle spindle
myocardium
myofibril
myofilament
myosin
neuromuscular junction
parasympathetic nervous system
perimysium
pleura
pleural pressure
power stroke
proprioceptor
proximal
pulmonary valve
Purkinje fibersP-wave QRS complex red blood cell repolarization right bundle branch sarcolemma sarcomere sarcoplasm sarcoplasmic reticulum semilunar valves sinoatrial (SA) node sliding-filament theory slow-twitch fiber superior sympathetic nervous system synovial fluid synovial joints systole tachycardia tendon tetanus trachea tricuspid valve tropomyosin troponin T-tubule T-wave twitch Type I fiber Type IIa fiber Type IIx fiber uniaxial joints vein venous system ventricle venule vertebral column Z-line
1. Which of the following substances regulates muscle actions? a. potassium b. calcium c. troponin d. tropomyosin 2. Which of the following substances acts at the neuromuscular junction to excite the muscle fibers of a motor unit? a. acetylcholine b. ATP c. creatine phosphate d. serotonin 3. When throwing a baseball, an athlete’s arm is rapidly stretched just before throwing the ball. Which of the following structures detects and responds to that stretch by reflexively increasing muscle activity? a. Golgi tendon organ b. muscle spindle c. extrafusal muscle d. Pacinian corpuscle 4. From which of the following is the heart’s electrical impulse normally initiated? a. AV node b. SA node c. the brain d. the sympathetic nervous system 5. Which of the following occurs during the QRS complex of a typical ECG? I. depolarization of the atrium II. repolarization of the atrium III. repolarization of the ventricle IV. depolarization of the ventricle a. I and III only b. II and IV only c. I, II, and III only d. II, III, and IV only